When we think of heart disease, we often imagine it as a jolt — a heart attack, a stroke, or a medical emergency that arrives without warning. But according to cardiologists, the real danger to your heart could be hiding in the patterns of your everyday life. From late-night snacking to endless screen time, skipped meals to excess salt, it’s our daily routines that may be damaging our cardiovascular health, regardless of age, gender, or body size.
“It is commonly believed that heart disease occurs only in older or obviously unfit individuals. Actually, cardiovascular disease can accumulate over years, maybe in young, thin, or ‘healthy-looking’ people. Heritability, stress, and lifestyle are factors, and prevention is the way to go,” Dr Vikrant Khese, Cardiologist, Apollo Clinic, Kharadi, tells Health Shots.
In recent years, the incidence of heart-related conditions in individuals below 50 years of age, has seen a rise. This busts the myth that heart disease is only for older people or men, says Dr Nitin Bote, Interventional Cardiologist, K.J. Somaiya Hospital and Research Centre.
“We are actually seeing an increasing number of young patients, including women, presenting with early symptoms of heart disease, caused by stress, lifestyle, and hormonal changes. Another myth is that if you take medication, lifestyle modifications are not required. This is very much not the case. Medication controls risk but long-term cardiac health relies on habit changes,” adds Dr Bote.
Here are some of the daily lifestyle habits that may silently raise cardiovascular risk:
Inadequate rest increases stress hormone levels and blood pressure, straining the heart. According to a 2010 study about sleep duration as a risk factor for cardiovascular disease, there was an increased risk of Congenital Heart Disease in subjects with sustained 5 or fewer, 6, 7, and 9 hours or more, compared with those with 8 hours of sleep.
If you spend hours on phones or in front of the TV, be mindful. Studies have found a correlation between excessive use of mobile phones and TV screens, and an increased risk of coronary artery disease, heart failure, and ischaemic heart disease. This is because these activities promote a sedentary lifestyle, affecting circulation and movement, and thereby raising the risk of obesity, which is not good for the heart.
Making a habit of late-night snacking can disrupt metabolism, impact insulin levels, and even add to weight and cholesterol issues.
According to Dr Bote, missing meals or consuming huge, irregular portions, can raise insulin levels and disrupt metabolic balance, indirectly impact cardiovascular health.
One of the most overlooked threats for your heart? Salt. Both Dr Khese and Dr Bote, agree that excessive salt is one of the biggest risks for heart damage. “Through processed snack foods, restaurant meals, or what may be perceived as benign condiments, most individuals take in twice the daily recommended amount of sodium,” says Dr Bote. Explaining the risks, Dr Khese adds, “Consuming salt in excess on a regular basis increases blood sodium concentrations that attract fluid into the blood vessels, causing them to swell. This is what increases blood pressure and causes the heart to work more forcefully, which can lead to hypertension, left ventricular hypertrophy (thickening of heart muscle), and eventually heart failure. Too much salt consumption also hardens arteries in the long term.”
Also read: 6 signs you’re eating too much salt
Want to take care of your heart? Give up or reduce sugary drinks, packaged snacks, and fried foods, which tend to increase inflammation and unhealthy cholesterol.
A lack of nutrient-dense foods means the body misses out on key antioxidants and heart-protective fibre. Your diet plays a key role in protecting your heart, so if you consume a high-trans fat diet with added sugar and red meat, with low fibre, fruit, and vegetable consumption, you may be inviting a cardiovascular risk, says Dr Khese.
Even normal-weight individuals are at risk for unfavourable lipid profiles, hypertension, and insulin resistance if they are sedentary. Sedentary life affects circulation, causes inflammation, and promotes the development of plaque in the arteries, independent of body size. “Everyday physical movement, even just walking, can dramatically lower cardiovascular risk,” asserts Dr Bote.
Long-term emotional stress can elevate blood pressure and contribute to hormonal imbalances that affect heart health.
Missing preventive screenings can delay diagnosis of high blood pressure, cholesterol, or early-stage heart disease.
Prevention is the best cure! So, making simple, sustainable shifts like eating more fibre, avoiding sugary beverages, sleeping well, managing stress, and even simply walking for 30 minutes daily — can dramatically reduce long-term heart disease risk.
Regular health check-ups, especially after the age of 30, are crucial to catch warning signs before they turn critical.
“Heart disease is preventable in most cases. By being mindful of what we eat, staying physically active, managing stress, and getting enough sleep, we can protect our hearts from damage that builds silently over time,” says Dr Bote.
With nutrient shortfalls widespread among expectant mothers in the UK, new research reveals why focused dietary advice, effective supplementation, and better policy could make all the difference for families across generations.
Image Credit: VectorMine / Shutterstock
In a recent briefing paper in the journal Nutrition Bulletin, researchers elucidate patterns of maternal nutrition during prenatal and perinatal periods among UK women. They aim to provide scientifically sound nutritional advice for prospective and new mothers, clinical professionals, and policymakers.
Findings reveal that most of the UK’s women fall short on essential nutrients, with these deficiencies pronounced in teenagers, women from lower-income households, ethnic minorities, smokers, those with multiple pregnancies, and those experiencing food insecurity. It identifies inconsistencies in nutritional advice received by women, even when following respected national guidelines.
The review acknowledges the surge in popularity of plant-rich diets but emphasizes that proactive management through fortified foods and targeted supplements (such as B12 and algal DHA) is essential to avoid key nutritional deficiencies. It calls for clear, consistent, and culturally appropriate guidance from healthcare professionals to optimise maternal and public health.
Pregnancy isn’t just about expecting a baby; it represents a critical time and a powerful opportunity to shape lifelong health. Decades of evidence have highlighted the strong link between the diet during pregnancy and long-term health outcomes for both the mother and her child. During prenatal and perinatal periods, women should focus on nutrient density over quantity, as they do NOT need to “eat for two”, prioritising diets rich in essential nutrients.
Research has established the crucial roles of protein, specific fatty acids, complex carbohydrates, and essential vitamins in supporting foetal growth, lactation, and minimizing gestation complications. Weight management (both pre-pregnancy BMI and gestational gain) is also increasingly recognized for its pregnancy impacts. Unfortunately, women often receive inconsistent advice, and reviews seeking to inform public health policy through nutrition guidance can be generic.
The work of Williamson’s 2006 review partially addressed this gap by investigating relationships between dietary intakes and pregnancy outcomes. This work updates Williamson’s findings with new data and examines potential discrepancies between UK dietary guidance and science-based nutrient priorities.
The British Nutrition Foundation (BNF) briefing builds upon Williamson’s study by leveraging UK national surveys, clinical guidelines, and systematic reviews to advise expectant mothers, healthcare professionals, and policymakers on key nutrient priorities during pregnancy. It identifies patterns and trends in the UK and evaluates how well national recommendations align with scientific evidence, aiming to support future policy reform.
The review focuses on four key areas: 1. Nutrient intakes, 2. Supplementation, 3. Food safety, and 4. Weight management. Study data were obtained from extensive UK survey datasets, the National Institute for Health and Care Excellence (NICE) clinical guidelines, and systematic reviews (Maternal & Child Nutrition, Nutrition Bulletin, and scientific journals).
The review conducted extensive nutrition monitoring by comparing survey data to UK recommendations, analysed demographic factors to identify high-priority groups, and evaluated how guidelines from NICE and the World Health Organization (WHO) align with current clinical evidence. It also examined the implications of different dietary patterns, assessed the impact of pre-pregnancy weight and gestational weight gain on health outcomes, and reviewed food safety by identifying dietary trends and high-risk foods.
UK survey data reveal that most pregnant women fail to meet the UK-recommended intakes of folate and iron (dietary and supplemental), with only 19.7% taking pre-conception folic acid supplements (400 µg/day). Vitamin D (10 µg/day advised during October to March) and iodine (UK RNI: 140 µg/day; EFSA recommends 200 µg/day during pregnancy) recommendations also reveal widespread shortfalls, underscoring a significant nutritional public health challenge.
Confusion arises not from UK guidelines but from inconsistent advice delivery and global variations. While NICE clearly recommends 10 µg/day vitamin D, other international bodies suggest different ranges. This inconsistency in global positions likely contributes to confusion among some professionals.
Suboptimal weight management is widespread, with over 20% of UK pregnant women entering pregnancy with obesity. Both insufficient and excessive gestational weight gain are problematic, with IOM guidelines providing BMI-specific targets. Excessive GWG is linked to gestational diabetes, hypertension, preeclampsia, preterm birth, and long-term obesity for mother and baby. These risks are even higher among vulnerable groups, including teens, low-income women, ethnic minorities, and those with multiple pregnancies.
On a more positive note, the review identified a positive trend of increased adherence to plant-based foods in the UK. While plant-based foods are known to support healthy pregnancies and are nutritionally adequate when well-planned, they may fall short in critical nutrients, such as vitamin B12, calcium, iodine, iron, and long-chain omega-3 fatty acids. Healthcare providers must proactively manage these potential deficiencies through dietary strategies (fortified foods), targeted supplementation (e.g., B12, algal DHA), and monitoring.
The present briefing paper by the BNF conveys a clear message – a balanced diet supplemented with specific nutrients (folic acid pre-conception, vitamin D, and DHA from 20 weeks) is essential for optimal outcomes. It emphasizes that nutrition advice must be specific, consistent, culturally appropriate, and supportive. It asks healthcare providers to ensure personalized interventions for pregnant women, especially those in high-vulnerability populations.
Weight management based on pre-pregnancy BMI, food safety education (including avoidance of liver, high-risk cheeses, and meats, and limiting caffeine intake to more than 200mg per day), and tailored advice for plant-based diets are all equally important. Bridging the gap between public health recommendations and lived dietary habits through accessible resources could dramatically improve maternal and infant outcomes across generations.
Journal reference:
In Indian farmland, chickpeas are not only an important protein source for the country’s vegetarian population but also account for 70% of the global total production. Driven by agricultural technological advancements and policies such as the national food security program, India’s chickpea production has surged from 7.3 million tons in 2014-2015 to 14 million tons in 2021-2022. However, this crop is facing a serious threat from Sclerotinia sclerotiorum-induced sclerotinia disease (commonly known as “white mold”). Under suitable temperature and humidity conditions, it can cause a yield reduction of over 50%. The pathogen survives long-term through sclerotia in the soil, making traditional control methods difficult to completely solve.
Biochar is a porous carbon material formed by the high-temperature pyrolysis of biomass under oxygen-deficient conditions. Its abundant pores provide a “shelter” for microorganisms, and its high carbon content supplies energy for beneficial bacteria. As a widely used biocontrol fungus, Trichoderma can inhibit pathogens by competing for nutrients and secreting antimicrobial substances, while also promoting plant root development. Can biochar serve as a high-quality carrier for Trichoderma to inhibit Sclerotinia sclerotiorum while promoting crop growth?
A study by Vipul Kumar from Lovely Professional University (India), and Rachid Lahlali from the National School of Agriculture of Meknès (Morocco) and their colleagues, provides an answer to this question. The paper was recently published in Frontiers of Agricultural Science and Engineering (DOI: 10.15302/J-FASE-2024598)
This study selected three common biomasses—hardwood, kitchen waste, and wheat straw—to prepare biochar, systematically compared their physicochemical properties (such as carbon-nitrogen content and pore structure), and observed the growth of Trichoderma on biochar and its inhibitory effect on Sclerotinia sclerotiorum by combining different concentrations and particle sizes. Field trials further verified the actual impact of these combinations on chickpea growth and disease.
The results showed that hardwood biochar performed excellently in multiple key indicators: it had the highest lignin and cellulose content, and its formed pore structure was more conducive to Trichoderma colonization; after 6 weeks, the number of Trichoderma on hardwood biochar reached 33.5×105 CFU/g, significantly higher than other types of biochar. More critically, the combination of hardwood biochar and Trichoderma exhibited a “dual effect”—it not only inhibited the growth of Sclerotinia sclerotiorum but also promoted chickpea root development, while reducing disease severity by 36.5%.
This is equivalent to creating a “livable community” for Trichoderma, enabling beneficial bacteria to more efficiently combat pathogens while improving the soil environment. Researchers noted that hardwood biochar is not only a “carrier” for Trichoderma; its inherent alkalinity and porous properties can directly inhibit the survival of Sclerotinia sclerotiorum, and the proliferation of Trichoderma further enhances this inhibitory effect. Field data showed that the treatment group applying hardwood biochar + Trichoderma had significantly increased phenolic substance content in chickpea leaves, indicating that the plants’ own disease resistance was also activated.
This study clarifies the optimal parameters for biochar as a biocontrol fungus carrier: hardwood source, 4% addition concentration, and 150-µm particle size. This provides an operable technical solution for practical agricultural applications, holding promise to reduce chemical pesticide use while improving chickpea yield and quality.
Researchers have found that the timing of when fluoxetine (commonly known by its brand name, Prozac) is administered is vital in determining the impact it has on long-lasting mood behavior and accompanying changes in the prefrontal cortex. The new study in Biological Psychiatry, published by Elsevier, provides crucial mechanistic insights into alterations in neurocircuits that regulate mood behavior, which are key to making informed choices in treating depression in children and adolescents.
Serotonin, the neurotransmitter that is modulated by selective serotonin reuptake inhibitors (SSRIs) like Prozac, is known to have a critical impact on neurodevelopment, influencing the fine-tuning and maturation of emotional neurocircuits. Due to its perceived favorable risk-benefit profile, Prozac is often the drug of choice for gestational and postpartum depression in mothers and treating childhood and adolescent depression.
Lead investigator Vidita A. Vaidya, PhD, Department of Biological Sciences, Tata Institute of Fundamental Research, Mumbai, India, explains “Using a rodent model, we addressed specific long-term behavioral, molecular, bioenergetic, and cytoarchitectural consequences of postnatal and juvenile fluoxetine treatment. We found that treatment with fluoxetine during early postnatal life in male, but not female rats, led to long-lasting increases in anxiety- and depression-like behaviors, whereas treatment during adolescence had the opposite effect, significantly reducing these behaviors. This was noted as long as six months after the cessation of drug treatment, highlighting that modulation of serotonin levels with SSRIs like Prozac in developmental windows can result in behavioral changes that are highly persistent.”
Co-investigator Utkarsha Ghai, PhD, Department of Biological Sciences, Tata Institute of Fundamental Research, Mumbai, India, adds, “The diametrically opposing influence of early postnatal and adolescence fluoxetine treatment on mood behavior was also noted in the completely different influence on gene expression, architecture of neurons, and bioenergetics (the brain’s energy levels) in the prefrontal cortex. While early postnatal fluoxetine resulted in a long-lasting decline in bioenergetic status in the prefrontal cortex, adolescent exposure increased bioenergetics, uncovering a previously unknown role for fluoxetine administration in specific developmental windows.”
The researchers point out that the impact on neuronal bioenergetics is likely critical, as the long-lasting increase in depressive behavioral responses noted with early postnatal fluoxetine treatment could be reversed by adult-onset nicotinamide (vitamin B3), a NAD+ precursor that enhances mitochondrial bioenergetics treatment.
John Krystal, MD, Editor of Biological Psychiatry, comments, “The notion that antidepressant effects may differ by sex and at different stages of development could be clinically important. It is interesting that the stark biological differences between fluoxetine effect among early postnatal and juveniles are limited to males. As we come to understand the human correlates of the changes observed here in rodents, it may become important to be able to prevent these effects. Thus, the finding that vitamin B3 (nicotinamide), which could easily be administered to boys exposed to fluoxetine, seems to prevent the metabolic and structural consequences of fluoxetine exposure in male rodents.”
Dr. Vaidya concludes, “The novelty of this research lies in the discovery of more than one sensitive window during postnatal life, during which perturbing serotonergic neurotransmission via fluoxetine can exert completely differing effects on mood behavior. While it is difficult to directly extrapolate the time windows in our studies with rodents to the exact equivalent human age, our results underscore the importance of considering both the temporal window of treatment and sex as key variables that can influence the molecular, cellular, bioenergetic, and behavioral outcomes of exposure to fluoxetine during vulnerable developmental stages. We believe this work may motivate further studies to carefully examine the influence of disruption of serotonin signaling in sensitive developmental epochs in both animal models and in clinical cohorts on mood behavior.”
Source:
Journal reference:
Ghai, U., et al. (2025). Postnatal and juvenile fluoxetine treatment evokes sex-specific, opposing effects on mood-related behavior, gene expression, mitochondrial function, and dendritic architecture in the rat medial prefrontal cortex. Biological Psychiatry. doi.org/10.1016/j.biopsych.2025.04.026.
A common bacteria found in the stomach could be fuelling millions of stomach cancer cases globally. A new study suggests this bacterial infection could cause nearly 12 million cancers among people born over a single decade.Scientists from the International Agency for Research on Cancer (IARC), part of the World Health Organisation, project that if current trends continue, around 15.6 million people born between 2008 and 2017 will be diagnosed with stomach (gastric) cancer in their lifetime. Of all those cases – 76%, i.e., a staggering 11.9 million, may be caused by the Helicobacter pylori bacteria (H. pylori), according to a study published in the journal Nature Medicine.Read on to know more.
Stomach cancer, often called a “silent killer,” is grabbing global attention following the striking new warning – thanks to the world’s most under-the-radar risk.
Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, flagellated, helical bacterium. Mutants can have a rod or curved rod shape that exhibits less virulence. This easily transmissible bacterium often shows no symptoms – which makes it more invincible.Let’s explore more.A common but concealed inhabitant: Half the world’s population hosts H. pylori in their stomach lining, often without visible symptoms. It’s classified as a class I carcinogen by IARC and the US Carcinogens Report.Transmission vectors: The bacterium spreads through contaminated food or water and close contact, like saliva or fecal-oral routes. It’s more prevalent in regions with poor sanitation and crowded living conditions, especially in Asia, Africa, and parts of Latin America.Silent but damaging: Though only 10–20% may show mild symptoms like indigestion or bloating, H. pylori quietly triggers chronic inflammation – setting the stage for ulcers, atrophic gastritis, and eventually cancer.
For the study, scientists examined the incidence of stomach cancer in 185 countries in 2022 and combined it with projections of future deaths.They looked at the potential impact of screen-and-treat strategies for H. pylori and found the number of stomach cancers could be cut by up to 75% overall.Asia accounts for two-thirds of projected future cases, with 10.6 million cases (68% of the total), followed by the Americas (2 million or 13%), Africa (1.7 million or 11%), Europe (1.2 million or 8%), and Oceania (0.07 million or 0.4%).The study projected that under current trends, 11.9 million people could be diagnosed with stomach cancer attributable to H. pylori infection by 2101, which is the year someone born in 2017 would turn 84.Dr. Jin Young Park, one of the study’s co-authors and head of the gastric cancer prevention team at the WHO’s International Agency for Research on Cancer (IARC), said: “It is essential that health authorities make gastric cancer prevention a priority and accelerate efforts to control it by planning pilot and feasibility projects, including H. pylori screen-and-treat programmes,” adding, “With demographic changes set to increase the gastric cancer burden in many parts of the world, there is an urgent need for coordinated prevention strategies and for regional health systems to be prepared to manage the growing burden.”
Stomach cancer is largely preventable, but the prognosis is poor once a patient is diagnosed. It is the fifth most common form of cancer worldwide, killing an estimated 770,000 people per year. As per the study, chronic infection with H. pylori is a major cause, and it helps explain the rise in stomach cancers among young people in recent years.The link between H. pylori and gastric adenocarcinoma is solid: infected individuals have a 2–6-fold greater risk. According to research, around 90% of stomach cancers are linked to this infection, and up to 89% of non-cardia gastric cancers may be due to H. pylori. Its presence is also tied to MALT lymphoma, with tumor regression observed after eradication.But how does a bug become a carcinogen?The bacterium’s virulence, especially strains containing the cagA gene and the cag pathogenicity island, intensifies inflammation and damages DNA repair mechanisms. Persistent inflammation produces reactive oxygen and nitrogen species, leading to DNA damage in gastric cells.Genetic susceptibility and co-factors: Not all infected individuals develop cancer. A study showed that certain genetic variants prompt immune-suppressive environments via IFNα, increasing cancer risk. Environmental risk factors – smoking, high salt intake, low fruit/vegetable diets, obesity, and genetic predispositions – can aggravate the damage.
Gastric cancer, also known as stomach cancer, is a disease where malignant (cancerous) cells form in the lining of the stomach. It’s a growth of cells that starts in the stomach, a muscular, sac-like organ in the upper abdomen that plays a key role in digesting food. Most stomach cancers are adenocarcinomas, which develop from the gland cells in the stomach’s inner lining.
While stomach cancer rates have declined in many parts of the world, it’s still a significant health concern, particularly in East Asia.Symptoms: Early-stage stomach cancer often doesn’t cause noticeable symptoms, but later stages can include pain or discomfort in the upper abdomen, heartburn, feeling full after small meals, nausea, vomiting, and weight loss.Risk Factors: Risk factors include Helicobacter pylori infection, diet (especially high salt and smoked/preserved foods), obesity, smoking, and family history of stomach cancer.
Screen-and-treat programs: The study highlights that national initiatives to screen for and eradicate H. pylori could reduce new stomach cancer cases by up to 75%. Eradication has already reduced gastric cancer risk by roughly 75% in treated populations.Effective treatment protocols: Current treatment involves two weeks of quadruple therapy: two antibiotics, a PPI, plus possibly bismuth. However, rising antibiotic resistance often requires multiple courses.Early detection boosts survival: In the US, early cancer diagnosis rates rose by 53% (2004–2021), improving survival to around 75% – compared to just 7% for late-stage detection. In regions with high H. pylori prevalence, targeted screening via endoscopy and breath/stool tests starting from age 40–50 is recommended.
A major analysis reveals which GLP-1 drugs deliver the best results for glucose control, weight loss, and side effect profiles, offering new clarity for diabetes care decisions.
Study: Efficacy and safety of GLP-1 agonists in the treatment of T2DM: A systematic review and network meta-analysis. Image Credit: ALIOUI MA / Shutterstock
In a recent study published in the journal Scientific Reports, a group of researchers ranked the glycemic, weight, cardiovascular, and safety outcomes of eight Glucagon-Like Peptide-1 Receptor Agonists (GLP-1 RAs) versus placebo and standard antidiabetic drugs in adults with Type II Diabetes Mellitus (T2DM) using a Bayesian network meta-analysis.
Every ten seconds, someone worldwide develops T2DM, a chronic condition that inflates household medical bills and doubles the risk of heart attack. Global prevalence is projected to climb to 643 million people by 2030, spurring an urgent search for treatments that lower glucose without promoting weight gain.
GLP-1 RAs stimulate insulin secretion and curb appetite, but clinicians face a crowded shelf of brands differing in dose, duration, and cost. Families, policymakers, and insurers all seek the treatment that maximizes benefits while minimizing drawbacks, highlighting the ongoing need for comparative research.
Investigators conducted a systematic review and Bayesian Network Meta-Analysis (NMA) in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses for Network Meta-Analyses statement and registered the protocol in the International Prospective Register of Systematic Reviews. PubMed, Cochrane Library, Embase, Web of Science, and Chinese databases were searched from inception to 2 October 2024.
Eligible studies consisted of randomized controlled trials (RCTs) involving adults with T2DM that lasted at least eight weeks and compared twice-daily Exenatide (EBID), once-weekly Exenatide (EQW), Semaglutide, Albiglutide, Lixisenatide, Dulaglutide, Liraglutide, or Tirzepatide against one another, placebo, or conventional antidiabetic therapies such as insulin, metformin, sodium-dependent glucose transporter 2 inhibitors, dipeptidyl peptidase-4 inhibitors, or sulfonylureas.
The analysis combined oral and injectable Semaglutide into a single category for statistical assessment, reflecting their similar efficacy.
Reviewers independently undertook study selection, data extraction, and Cochrane risk-of-bias assessment, resolving disagreements by consensus. The analysis first assessed changes from baseline in Glycosylated Hemoglobin A1C (HbA1c) and Fasting Plasma Glucose (FPG).
Additional endpoints encompassed body weight, Body Mass Index (BMI), systolic and diastolic blood pressure (SBP, DBP), total cholesterol (TC), high-density and low-density lipoprotein cholesterol (HDL-C, LDL-C), and any reported adverse events.
Results were pooled as mean differences (MD) or risk ratios (RR) with 95% confidence intervals (CIs). Whenever between-study variability (I²) exceeded 50%, a random-effects model was employed, and heterogeneity was evaluated using the Chi-squared test.
Sixty-four eligible trials, including 25,572 participants, formed a dense evidence network. Compared to placebo, every GLP-1 RA reduced HbA1c, yet the effect size varied sharply.
Tirzepatide achieved the greatest absolute drop (MD −2.3 percentage points, 95 % CI −2.7 to −1.9), followed by Semaglutide (−1.5) and Liraglutide (−1.2); Lixisenatide’s reduction of −0.56 ranked last.
When benchmarked against traditional drugs pooled across insulin, Metformin, Sodium-Dependent Glucose Transporter 2 inhibitors, Dipeptidylpeptidase-4 inhibitors, and sulfonylureas, only Tirzepatide (−1.5), Semaglutide (−0.73), Liraglutide (−0.40), Dulaglutide (−0.34), and EQW (−0.36) retained statistical superiority.
For FPG, the hierarchy was similar: Tirzepatide lowered levels by −3.1 millimoles per liter, Semaglutide by −2.0, and Liraglutide by −1.6 millimoles per liter, compared to placebo; short-acting agents and Albiglutide produced a minimal change. The Surface Under the Cumulative Ranking Curve analysis assigned Tirzepatide a 100% probability of occupying the top position for both glycemic outcomes.
The therapies diverged further on weight. Against placebo, Tirzepatide resulted in a weight loss of −9.1 kilograms, Semaglutide −2.8, EBID −1.8, and Liraglutide −1.2; other agents were weight-neutral. Notably, EBID resulted in greater weight loss than liraglutide in this comparison.
Compared to conventional treatment, every GLP-1 RA except Albiglutide reduced weight, with Dulaglutide and Lixisenatide also demonstrating significant weight reduction. Tirzepatide’s −10 kilograms again led the field.
Blood Pressure, BMI, and lipid fractions showed no statistically significant differences across interventions, implying that glycemic and weight advantages occur without observed short-term changes in cardiovascular parameters. Albiglutide was found to be ineffective in improving weight outcomes versus traditional drugs.
Gastrointestinal complaints constituted the dominant safety signal. Semaglutide, Dulaglutide, Liraglutide, Lixisenatide, and Tirzepatide each tripled the risk of nausea and vomiting compared to placebo; the risk approximated parity when compared with legacy drugs already notorious for gastrointestinal intolerance.
Hypoglycemia profiles diverged: EBID and Semaglutide increased episodes (RR 3.3 and 4.6, respectively) relative to placebo, whereas Liraglutide and Lixisenatide significantly reduced the risk compared with traditional regimens.
Other adverse events, including nasopharyngitis, headache, and elevations in lipase, did not differ materially. Node-splitting and loop inconsistency tests revealed no significant incoherence between direct and indirect evidence, and funnel plots were symmetrical, supporting the credibility of pooled estimates.
Collectively, the analysis crowned Tirzepatide as the most potent agent for glucose lowering and weight loss, with Semaglutide a consistent runner-up. Tirzepatide’s dual agonism of GIP and GLP-1 receptors may underpin its superior efficacy.
Liraglutide delivered moderate glycemic benefits coupled with a neutral or protective hypoglycemia footprint, which may be advantageous for leaner or older adults at risk of underweight or hypoglycemia, suggesting a niche for patients intolerant to Semaglutide or at high hypoglycemic risk.
Short-acting formulations and Albiglutide rarely dominated any outcome, underscoring the clinical shift toward once-weekly or dual-agonist molecules. These rankings remained stable across subgroup and sensitivity analyses, bolstering confidence in their relevance for clinicians.
To summarize, long-acting GLP-1 RAs outshine older therapies by combining robust glucose control with meaningful weight loss in adults living with T2DM.
This NMA shows that Tirzepatide delivers the strongest overall profile, followed closely by Semaglutide, while Liraglutide balances efficacy with the lowest risk of hypoglycemia. Short-acting agents and Albiglutide offer limited additional value. Clinicians should consider a patient’s weight goals, gastrointestinal tolerance, and susceptibility to hypoglycemia when selecting among agents.
Policymakers and payers can prioritize Tirzepatide or Semaglutide for obesity-related diabetes, reserving Liraglutide for individuals with leaner body types or those who are sensitive to hypoglycemic episodes in everyday clinical practice worldwide.
Journal reference:
July 8, 2025
TOKYO – A young resident of Kanagawa Prefecture visited the 2025 Osaka-Kansai Expo on the same day that he developed symptoms of the measles, the prefectural government said Saturday.
Aged from 10 to 19, the person is a resident of Hiratsuka in the prefecture and went to the Expo on June 21, according to the prefectural government. The Kanagawa and Osaka prefectural governments are calling for anyone who visited the venue on the same day and developed a fever or other symptoms to contact a medical facility about possible treatment.
The resident traveled to Osaka by car and took a shuttle bus from a parking lot in Sakai, Osaka Prefecture, from about 8 a.m. to 8:30 a.m. to the Expo venue, according to the Kanagawa prefectural government and others.
He visited eight pavilions, including those for the European Union and Cambodia, from around 9 a.m. to 3 p.m. He then returned to the parking lot via shuttle bus from around 3 p.m. to 3:30 p.m.
The young person had a fever and a headache on the day that he visited the Expo. As he also developed a rash, he visited a medical institution on June 25 and 27. Genetic testing by the Kanagawa Prefectural Institute of Public Health confirmed Thursday that he had contracted measles.
He has no history of overseas travel and how he became infected is unknown, according to the prefectural government.
As of June 29, a total of 32 people had been confirmed to have contracted measles in Kanagawa Prefecture this year, the institute said.
Measles is highly contagious and spreads through the air. It can be transmitted through droplets from coughing or sneezing, as well as by direct contact with an infected person.
When the virus enters the body of a person who is not immune, symptoms such as a fever, cough and rash appear within 10 to 12 days in most cases. Measles can cause pneumonia and encephalitis and is said to be fatal in 1 in 1,000 cases.
Just washing one’s hands and wearing a mask cannot fully prevent infection. Receiving two doses of vaccine is considered effective.
The World Health Organization verified that Japan had eliminated endemic measles transmission in 2015, but new cases have continued to be confirmed. According to the Japan Institute for Health Security, 156 cases of infection had been confirmed nationwide this year as of June 22.
The Expo visitor who tested positive had received two doses of vaccine.
“People who have been vaccinated twice will excrete fewer viruses. If you experience symptoms such as fever or rash, please consult a medical institution before seeking treatment,” said Atsuo Hamada, a specially appointed professor at Tokyo Medical University and an expert on travel medicine.
NEW DELHI: Commonly prescribed medications for anxiety, depression and sleep disorders may be associated with a higher risk of developing amyotrophic lateral sclerosis (ALS), a progressive and fatal neurological disorder, according to a new study recently published in JAMA Neurology.The study examined the use of anxiolytics (used to relieve anxiety), hypnotics and sedatives (used to aid sleep or calm the body), and antidepressants (which work by altering brain chemistry to improve mood). Researchers found that individuals who were prescribed these medications were more likely to be diagnosed with ALS later in life compared to those who did not take them.Significantly, the study also found that people who used these medications before being diagnosed with ALS had a poorer prognosis, meaning their disease progressed more quickly and survival was shorter. However, experts caution that this finding is based on association, not causation.“These medications are often prescribed for symptoms such as anxiety, sleep disturbances, or depression, which may appear during the early (prodromal) phase of ALS – well before a formal diagnosis,” explained Dr M S Panduranga, senior consultant (neurology), Dharamshila Narayana Superspecialty Hospital. “So, the link may reflect early, subtle neurological changes rather than the harmful effect of the drugs themselves.”The study, conducted in Sweden, analysed nationwide data from over 1,000 ALS patients and more than 5,000 healthy individuals using the Swedish Motor Neuron Disease Quality Registry. The average age of participants was 67.5 years, and just over half (53.1%) were male.Dr Manjari Tripathi, professor and head of neurology at AIIMS, explained that most neuropsychiatric medications act on the brain’s inhibitory pathways, which could interfere with motor neuron activity. “There could also be a toxic effect, especially with long-term, consistent use – not just occasional doses,” she said.“Motor neuron disease leads to slow but steady progression of muscle weakness,” she added. “Patients begin to struggle with everyday tasks – buttoning a shirt, combing their hair, walking. Eventually, they become wheelchair bound. Swallowing and speech become difficult, and muscles visibly shrink.” One type of ALS, she noted, was the same condition renowned physicist Stephen Hawking lived with for decades.While the exact timeline between medication use and ALS onset remains unclear, Dr Madhukar Bhardwaj, director and head of neurology, Aakash Healthcare, said that a longer history of psychiatric symptoms and prolonged medication use appears to be associated with increased ALS risk.“In some observational studies, individuals using anxiety or depression medications for more than 10 years showed a stronger link with ALS, especially in younger patients,” he said. “It’s not yet certain whether this reflects a true biological risk or simply earlier diagnosis due to more medical attention.”“While there’s no definitive proof that these medications cause ALS, we need to be cautious, especially when prescribing them to individuals with signs of neurological disease,” said Dr Anshu Rohatgi, vice-chairperson (neurology), Sir Ganga Ram Hospital.Doctors emphasise that patients should not stop their medications on their own. Instead, they should speak with their healthcare providers if they have concerns.
SINGAPORE, July 7, 2025 /PRNewswire/ — SCG Cell Therapy Pte Ltd (SCG), a clinical-stage biotechnology company pioneering TCR T cell therapy for infectious diseases and associated cancers, announced today that the China National Medical Products Administration (NMPA) has cleared the Investigational New Drug (IND) application for SCG101V, marking the first-ever investigational cell therapy to enter regulatory approved Phase 1/2 clinical trial for chronic hepatitis B virus (HBV) infection.
SCG101 is designed to cure chronic hepatitis B by eliminating HBV cccDNA and HBV-DNA integration within HBV-infected hepatocytes, which are the fundamental source of persistent infection and antigen production. These infected hepatocytes serve as the long-term viral reservoir that current antiviral therapies fail to eradicate. “SCG101 is designed to mimic the natural immune response observed in individuals who are able to clear HBV infection spontaneously. HBV-specific T cells play a central role in this process and, remarkably, through genetic engineering of T cells, we were able to replicate this natural process as demonstrated in our preclinical models and clinical data in hepatocellular carcinoma, providing strong evidence that this promise holds true in hepatitis B patients”, said Professor Ulrike Protzer, Scientific Founder of SCG Cell Therapy and Director of Institute of Virology Technical University of Munich / Helmholtz Munich.
In Phase 1 clinical trial of SCG101 in patients with HBV-related hepatocellular carcinoma (HCC), SCG101 demonstrated a good safety profile and sustained clearance of serum hepatitis B surface antigen (HBsAg), even in heavily pre-treated patients. Among the treated patients, 94% of patients had previously received nucleoside analogue (NA) antiviral therapy, and 72% presented with baseline liver cirrhosis. Following a single infusion of SCG101, all patients experienced a rapid decline in HBsAg level. Notably, 94% achieved a 1.0–4.6 log₁₀ reduction in HBsAg within 28 days, with HBsAg levels remained <100 IU/mL for up to one year without rebound. Furthermore, 23% of patients achieved complete HBsAg loss, a critical benchmark for a cure.
Professor Niu Jinqi, Vice President and Chief Physician of The First Hospital of Jilin University, commented: “SCG101 has demonstrated significant breakthrough potential in HBV-related liver cancer, remarkably, achieving HBsAg loss following a single dose. This IND approval by the NMPA marks a pioneering step toward a functional cure for chronic hepatitis B. We are excited about the prospects of this therapy and the benefit it could bring to millions of patients, helping to reduce the burden of liver disease in China and globally”.
Chronic HBV infection affects an estimated 300 million people globally and is a leading cause of liver cirrhosis and hepatocellular carcinoma, contributing to more than 820,000 deaths each year. While current standard-of-care therapies can suppress viral replication, they rarely achieve a functional cure and therefore cannot fundamentally halt disease progression.
“This IND clearance represents a historic milestone—not only for SCG but for the broader field of hepatitis B treatment. With indications across HBV-related hepatocellular carcinoma, HBV-related cholangiocarcinoma, and chronic hepatitis B, this IND clearance further validates our development strategy—expanding from virus-induced cancers to chronic infectious diseases“, said Christy Ma, Chief Executive Officer of SCG Cell Therapy. “SCG101 is the first cell therapy product to receive regulatory approval to enter a Phase 1/2 clinical trial specifically for HBV and HBV-induced cancer, and we are proud to lead the way in advancing toward a long-term functional cure. We remain on track for initiation of a pivotal study, following the recent completion of our Phase 1 study in patients with HBV-HCC. We look forward to sharing additional clinical data as we continue to push the boundaries of what’s possible in cell therapy.”
– END –
About SCG101
SCG101 is an investigational autologous T cell receptor (TCR) T cell therapy designed to selectively target specific epitope of the hepatitis B surface antigen (HBsAg). Powered by SCG’s proprietary GianTCR™ screening platform, which enables the discovery of natural, high-affinity, high-avidity TCRs against intracellular antigens presented via the major histocompatibility complex (MHC). SCG101 delivers precise immune-mediated clearance of infected and malignant cells demonstrating significant tumour inhibition and the eradication of HBV covalently closed circular DNA (cccDNA) in preclinical and clinical studies.
About HBV
Hepatitis B is a potentially life-threatening liver infection caused by the hepatitis B virus (HBV). HBV can cause chronic infection which leads to a higher risk of death from cirrhosis and liver cancer. Chronic HBV infection is a major global health issue, affecting nearly 300 million people across the world. Approximately 1.1 million people die every year from complications related to chronic HBV infection despite the availability of effective vaccines and current treatment options.
About SCG Cell Therapy
SCG Cell Therapy is a leading biotechnology company dedicated to developing novel immunotherapies for infectious diseases and associated cancers. The company focuses on targeting some of the most common cancer-causing infections, including Helicobacter pylori, HPV, HBV, and EBV. SCG is advancing a broad pipeline of TCR-based therapeutics aimed at preventing and curing infection-related cancers. Headquartered in Singapore, SCG operates across Singapore, China, and Germany, leveraging regional strengths to cover the entire value chain, from innovative drug research and discovery to manufacturing, clinical development, and commercialization. For more information, please visit www.scgcell.com.
SOURCE SCG Cell Therapy Pte Ltd